POLYMORPHISM OF ANGIOTENSIN I TYPE 1 RECEPTOR GENE IN ELDERLY PATIENTS WITH ESSENTIAL HYPERTENSION

Objective To detect the A/C1165 polymorphism of angiotensin Ⅱ type Ⅰ receptor (AT1-R)gene in essential hypertensive elderly. Methods The A/C1166 polymorphism of AT1-R gene was assessed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in a case-control study of 87 essential hypertensive elders (EH) and 55 normolensive elders (NT). Results The genotype frequencies of AA, AC, CC were 0 .805 , 0.161, 0 .034 in EH group and 0 .927 ,0 .073 ,0 .000 in NT group respectively. The frequency of C61166 allele was higher in EH group (0.115) than in NT group (0 .036 )(P<0 .05 ). Conclusion The resultsindicate that A/C1166 polymorphism of AT1-R gene may be associated with essential hypertension in elderly.     

老年原发性高血压AT1一R基因多态性的研究

目的 研究老年原发性高血压(EH)血管紧张素Ⅱ型受体(AT1一R)基因A／C1166多态性的特征。方法 应用聚合酶链反应一限制性片段长度多态性(PCR—RFLP)技术检测87例汉族老年EH患者和55例正常老年人的AT1－R基因A/C1166多态性分布。结果87例老年EH患者的C1166等位基因频率为0．115,55例正常老年人为0．036,经统计学分析两组间有显著差异(P<0．05)。结论老年EH的患者C1166等位基因频率明显升高,可能为EH发病的危险因素。     

Construction of shRNA Targeted to the Rat Angiotensin Ⅱ Type 1 Receptors and Its RNAi in Cytoplasma

Though remarkable progress has been madeinhypertension mechanisms in the last few decades ,the target of treating essential hypertension is stillfocusing pri marily on the rennin-angiotensin-aldo-sterone system(RAAS) .RAAS promotes vascularsmooth muscle constriction, remodels the struc-ture and function of the vascular system,enhancessodiumreabsorption in the kidney by sti mulatingaldosterone secretion. Therefore , RAAS is a cen-tral regulator of hypertension and plays a key roleinthe path…     

Angiotensin Ⅱ type 1 receptor modulation of L-type calcium currents in guine a-pig ventricular cells

Objective To study the cellular mechanism of the effect of Ang Ⅱ on I(Ca,L)in sing le guinea-pig ventricular cells by using losartan and 1-(5-Isoquinolinylsulfo nyl)-2-Methyl-Piperazine (H-7) as the Ang Ⅱ type 1 receptor (AT(1)) inhibit or and protein kinase C inhibitor, respectively.Methods Patch clamp techniques were used to study the cellular mechanism of the effect o f Ang Ⅱ on I(Ca,L) in single guinea-pig ventricular cells.Results In the whole cell patch clamp recording model, Ang Ⅱ stimulated I(Ca,L) in a concentration dependent manner; the maximal effect was obtained at 100 nmol/ L (n=9). At 30 nmol/L, Ang Ⅱ stimulated peak I(Ca,L) from 11.3±0.6 pA /pF to 15.3±0.6 pA/pF (at +10 mV, n=9, P&lt;0.05). 100 nmol/L Losartan, a specific AT(1) receptor inhibitor, had no effect on I(Ca,L) (n=9), but th e effect of Ang Ⅱ on I(Ca,L) was inhibited by 100 nmol/L Losartan. Ang Ⅱ on I(Ca,L) was also inhibited by 20 μmol/L H-7, a specific protein kinas e C inhibitor, whereas H-7 alone has no effect on I(Ca,L) (n=9).Conclusion Ang Ⅱ stimulates I(Ca,L) in guinea-pig ventricular cells by binding to AT 1 through a transduction pathway involving protein kinase C.     

Role of angiotensin Ⅱ and angiotensin Ⅱ receptors in vascular smooth muscle cell migration in vitro

ObjectiveTo determine the biotic effects of angiotensin Ⅱ (Ang Ⅱ) on the migration of rat smooth muscle cells (VSMCs) and investigate the mechanisms involved in the development of vascular injury. Methods VSMCs isolated from aortic media of Wistar rats and cultured by the modified explant method were adopted. In the presence and absence of Ang Ⅱ, the expression of Ang Ⅱ receptor (ATR) and reorganization of the actin cytoskeleton and focal adhesion of VSMCs were studied by an immunocytochemistry technique and fluorocytochemistry technique. Migration assays were performed with a modified Boyden’s chamber. The effects of AT(1)R antagonist (CV- 11974), AT2R antagonist (PD123319) on the aforementioned target were studied. Results VSMCs migration was stimulated by adding Ang Ⅱ. The dynamic reorganization of actin cytoskeleton and focal adhesions may be an important mechanism by which Ang Ⅱ facilitates VSMCs motility. The expression of AT(1)R in VSMCs could be upregulated initially after treatment with Ang Ⅱ, then decreased gradually. The expression of AT(1)R was downregulated by AT(1)R antagonists. The effect of Ang Ⅱ on VSMCs migration was mediated by AT(1)R, while AT2R had no significant effect. Conclusions The dynamic reorganization of focal adhesions and the actin cytoskeleton is required for Ang Ⅱ- induced VSMCs migration. This effect is mediated by AT(1)R.     

Gene polymorphisms of the renin-angiotensin system in essential hypertension

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The dynamic changes of angiotensin Ⅱ and atrial natriuretic factor levels in hypothalamus and infarct volume of rats with foc

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Effects of metoprolol on β1 adrenergic receptor polymorphism and receptor density in urban Chinese patients with heart failure

β-blockers have been recommended as a standard treatment for patients with mild to moderate systolic chronic heart failure （CHF） because they not only relieve patients＇ symptoms but also decrease mortality. However, β-blockers have a variety of effects on different CHF patients. Among them, β1-adrenergic receptor （AR） gene polymorphism is probably a significant one. The purpose of this study was to investigate the effects of metoprolol on cardiac function, cardiac geometrical size and density of β1-AR of CHF patients as well as the association between two common single nucleotide polymorphisms （SNPs） of β1-AR（Gly389Arg and Ser49Gly） and the effects of metoprolol.     

Effects of Xuezhikang (血脂康) and pravastatin on circulating endothelial progenitor cells in patients with essential hypertension

Objective:To investigate the impacts of Xuezhikang(血脂康,XZK)or pravastatin combined with antihypertensive drugs on circulating endothelial progenitor cells(CEPCs)in essential hypertensive (EH)patients.Methods:Eighty-eight EH patients were enrolled into the study and randomly assigned to the antihypertensive drug treatment group(ATH group,29 cases),the pravastatin treatment group(PRA group,29 cases)and the Xuezhikang treatment group(XZK group,30 cases).Patients in the 3 groups were treated with routine ant...     

高血压合并冠心病与AT1R基因多态性的关系

目的探讨血管紧张素Ⅱ的1型受体(AT1R)基因多态性与高血压患者合并冠心病(CAD)的关系.方法采用PCR-RDLP法,检测123例高血压患者(其中48例合并冠心病)和148例健康对照的AT1R基因型.结果高血压患者中无论是否合并冠心病,其AT1RA1166C基因型分布均与对照组无显著性差异(均为P＞0.05).高血压合并冠心病组与无冠心病组之间的AT1R基因型分布亦无显著差异(P＞0.05).结论AT1R基因A1166C多态性与中国人高血压病发生及高血压患者是否易患冠心病无关.     

早发冠心病与血管紧张素Ⅱ-1型受体A1166/C基因多态性的相关性研究

目的：研究血管紧张素Ⅱ－1型受体（AT1R）基因A1166／C多态性与中国早发冠心病（CHD）发生的相关关系及其对血脂水平的影响。方法：采用聚合酶链反应一限制性片段长度多态性（PCR－RFLP）分子生物学方法,检测71例早发CDH患者,76例迟发CHD患者和119例健康对照者的AT1R基因型;并按常规方法测定血脂水平。结果：共检测出2种AT1R基因型,分别是AA型和AC型,早发CHD组及迟发CHD组AA基因型（97．2％,92．1％）和AC基因型（2．8％,7．9％）频率与对照组（94．1％,5．9％）相比差异均无统计学意义。等位基因A和C频率在3组间差异无显著意义。AT1R基因多态性与血脂水平无关。结论：AT1R基因A1166／C多态性与早发CHD的发生发展似无直接关系。     

1型血管紧张素Ⅱ受体基因多态性与2型糖尿病伴高血压的相关性

目的：探讨1型血管紧张素Ⅱ受体（AT1R）基因多态性与2型糖悄病伴高血压之间的相互关系。方法：以AT1R基因为候选基因，应用PCR方法，检测132例2型糖尿病伴高血压患者及107例2型糖尿病无高血压患者的AT1R基因多态性。结果：2组研究对象AA基因型分布频率分别为88．79％与96．97％，AC基因型分布频率分别为11．21％与3．03％，A等位基因携带率分别为94．39％与98．48％，C等位基因携带率分别为5．61％与1．52％，均有显著性差异（P＜0．05），提示AT1R基因多态性与2型糖尿病伴高血压的发生有相关性，且糖尿病伴高血压患者病程显著延长，正常血压糖尿病患者与单纯舒张压升高糖尿病患者之间AT1R－A1166－C基因多态性无显著差异，而与单纯收缩压升高糖尿病患者之间有显著性差异，结论：AT1R基因参与型糖悄病伴高血压的发病，并仅与收缩压升高有关。     

血管紧张素原基因M235T和血管紧张素受体1基因A1166C多态性与飞行员原发性高血压的相关性

目的探讨血管紧张素原（AGT）基因M235T和血管紧张素受体1（AT1R）基因A1166C多态性与飞行员原发性高血压的相关性,为飞行员原发性高血压的预防提供依据。方法用聚合酶链反应（PCR）和限制性酶切检测48例飞行员原发性高血压患者和50例飞行员健康对照者的AGT M235T和AT1R A1166C多态性。结果飞行员高血压组AGT M235基因型和等位基因频率与健康对照组有明显差异,而AT1R A1166C两组间差异无统计学意义。结论 AGT M235T基因多态性与飞行员原发性高血压相关。     

原发性高血压患者血管紧张素Ⅱ-1型受体基因多态性

目的研究血管紧张素Ⅱ-1型受体基因多态位点A1166C与原发性高血压的关系。方法采用聚合酶链反应技术（PCR）对48名40岁以上成人和39例原发性高血压患者血管紧张素Ⅱ-1型受体（AT1R）基因多态性进行检测。结果 AC基因型、C等位基因频率高血压组与健康人群对照组差别无统计学意义（χ2=0.026、0.023,P〉0.05）。结论血管紧张素Ⅱ-1型受体基因可能与原发性高血压发病无关。     

血管紧张素Ⅱ—1型受体基因多态性与老年原发性高血压水平的关系

目的研究血管紧张素Ⅱ-1型受体(ATl-R)基因A/C1166多态性与老年原发性高血压(EH)血压水平的关系。方法应用PCR-RFLP技术检测87例老年EH患者和55例正常老年人的AT1-R基因A/C     

原发性高血压血管紧张素Ⅱ-1型受体基因与血压昼夜节律的相关性

目的：探讨血管紧张素Ⅱ-1型受体（angiogenesisIItypelreceptor，AT1R）基因1166位点多态性与原发性高血压（EH）及血压昼夜节律的关系。方法：选择EH患者100例，血压正常者80例，采用聚合酶链反应、限制性内切酶酶解及电泳分型的方法对AT1R基因1166位点的多态性进行分析；同时检测24h动态血压。结果①EH组中1166C等位基因频率明显高于对照组（P〈0．05）。②非杓型者比杓型者夜间收缩压、舒张压均增高（P〈0．05），1166C等位基因频率亦明显增高（P〈0．05）。结论：AT1R基因1166位点多态性与EH相关，1166C等位基因是EH发病的危险因素；AT1R基因A1166C多态性与血压昼夜节律的调节相关。     

ADAMTS-1基因多态性与汉族人群原发性高血压相关性研究

目的探讨汉族人群原发性高血压与含血小板反应素的去解联金属蛋白酶1（ADAMTS-1）基因启动子区rs402007（G/C）位点多态性的关联。方法提取汉族469例原发性高血压患者和229例血压正常的健康体检者（正常对照组）外周血液中的基因组DNA。采用多聚酶链反应和基因测序法对包含rs402007多态性位点在内的ADAMTS-1基因-99/+447目的片段进行基因检测,并进行Hardy-Weinberg平衡检验,检测研究群体有无群体代表性。结果原发性高血压组rs402007位点GC+CC基因型频率、C等位基因频率均高于正常对照组,差异均有统计学意义（均P＜0.05）。校正危险因素后,两组间GC+CC基因型频率差异仍有统计学意义（P=0.028,OR=1.809,95%CI：1.067~3.067）。结论ADAMTS-1基因rs402007位点多态性与汉族人群原发性高血压患病相关,C等位基因可能是原发性高血压的易感等位基因。     

1型血管紧张素Ⅱ受体基因多态性与2型糖尿病伴高血压的相关性

目的 探讨1型血管紧张素Ⅱ受体(ATIR)基因多态与2型糖尿病病伴高血压之间的相互关系。方法 以ATIF基因为侯选基因,就用PCR方法,检测132例2型糖尿病伴高血压２型糖尿病无高血压患者的ATIR基因多态性。结果２组研究对象AA基因型分布频率分别为88.79%与96.97%基因型分布频率分别为11.21%3.03%;A等位基因携带率分别为94.39%与98.48%,C等位基因携带率为5.61与1.52%,均有显著性差异(P＜0.05),提示ATIR基因多态性与２M糖尿病伴高血压的发生有相关性,且糖尿病伴高血压患者病程显著延长。正常血压糖尿病患者与单纯舒张压升高糖尿病患者之间ATIR-A1166-C基因多态性无显著差异,而与单纯收缩压升高糖尿病患者之间有显著性差异,结论,ATIR基因参与2型糖尿病伴高血压的发病,并仅与收缩压升高有关。     

高血压病患者ACE I/D基因多态性与胰岛素抵抗的关系

目的 研究高血压病患者血管紧张素转换酶(angiotensin converting enzyme ,ACE)基因 I/D多态性与胰岛素抵抗的关系.方法 用PCR方法检测300例汉族原发性高血压(essential hypertension ,EH)患者ACE基因 I/D多态性,并做空腹血糖、空腹胰岛素(fasting insulin ,FIN)检测,根据ACE基因 I/D多态性分组比较胰岛素抵抗情况,再根据胰岛素抵抗情况分组比较I/D多态性分布情况.结果 DD和ID型的胰岛素抵抗指数(HOMA-IR)显著高于Ⅱ型, DD型FIN显著高于Ⅱ型.EH胰岛素抵抗组DD型频率显著高于EH无胰岛素抵抗组.EH胰岛素抵抗组D等位基因频率显著高于EH无胰岛素抵抗组.结论 高血压病患者胰岛素抵抗情况与ACE基因I/D多态性有关,D等位基因为胰岛素抵抗的危险因素.